beta-endorphin and Weight-Gain

The literature mostly indicates that docking fat-tailed lambs initially reduces growth but that post-weaning growth and feed conversion efficiency then increase. The amount of fat deposited, the total separable lean meat to fat ratio and the meat quality all increase, while the percentage of bone in the carcase either decreases or does not change in the carcases of the docked lambs. Wool growth and characteristics are, in general, not affected and reproductive traits in ewes and lambs are improved by docking. The rectal temperature, respiration rate and pulse rate are decreased following docking. The concentrations of immunoreactive beta-endorphin and cortisol in the plasma and the incidence of foot stamping and restlessness, as indicators of stress, increase after docking. Other constituents of the blood are not significantly altered following docking or by the methods of docking. Docking of fat-tailed sheep using rubber rings at one day of age can be recommended.

Topics: Animal Husbandry; Animals; beta-Endorphin; Body Temperature; Eating; Female; Heart Rate; Hydrocortisone; Male; Meat; Reproduction; Respiration; Sheep; Tail; Weight Gain; Wool

Because the poor growth performance of intensively housed pigs is associated with increased circulating glucocorticoid concentrations, we investigated the effects of glucocorticoid suppression by inducing a humoral immune response to ACTH on physiological and production variables in growing pigs. Grower pigs (28.6 +/- 0.9 kg) were immunized with amino acids 1 through 24 of ACTH conjugated to ovalbumin and suspended in diethylaminoethyl (DEAE) dextran-adjuvant or adjuvant alone (control) on d 1, 28, and 56. The ACTH-specific antibody titers generated suppressed increases in cortisol concentrations on d 63 in response to an acute stressor (P = 0.002; control = 71 +/- 8.2 ng/mL; ACTH-immune = 43 +/- 4.9 ng/mL) without altering basal concentrations. Plasma beta-endorphin concentrations were also increased (P < 0.001) on d 63 (control = 18 +/- 2.1 ng/mL; ACTH-immune = 63 +/- 7.3 ng/mL), presumably because of a release from negative feedback on the expression of proopiomelanocortin in pituitary corticotropes. Immunization against ACTH did not alter ADG (P = 0.120; control = 1,077 +/- 25; ACTH-immune = 1,143 +/- 25 g) or ADFI (P = 0.64; control = 2,719 +/- 42; ACTH-immune = 2,749 +/- 42 g) and did not modify behavior (P = 0.681) assessed by measuring vocalization in response to acute restraint. In summary, suppression of stress-induced cortisol responses through ACTH immunization increased beta-endorphin concentrations, but it did not modify ADG, ADFI, or restraint vocalization score in growing pigs.

Topics: Adrenocorticotropic Hormone; Analysis of Variance; Animals; Antibodies; beta-Endorphin; Eating; Housing, Animal; Hydrocortisone; Immunization; Male; Population Density; Random Allocation; Swine; Time Factors; Vocalization, Animal; Weight Gain

Neonatal treatment with monosodium glutamate (MSG) decreases proopiomelanocortin (POMC) peptides and results in obesity. The yellow mouse is a model of obesity induced by the viable yellow (Avy) gene at the agouti locus on Chromosome 2, which results in overproduction of a POMC receptor antagonist. Thus we hypothesized that MSG, when imposed on the genetically susceptible model, would alter the development of obesity. Both yellow obese (Avy) and black lean (alpha/alpha) males were injected on Postnatal Days 1, 3, 5, 7, and 9 with 2.0 mg/g body weight MSG or saline SC. Their food intake, growth parameters, and neurochemical status were examined. Paradoxically, MSG interacted with the yellow phenotype to delay the rapid rate of weight gain characteristic of this model (p < 0.05). Food intake was decreased (p < 0.05) in both phenotypes treated with MSG, as was hypothalamic content of dopamine (p < 0.05) and of the POMC peptide, beta-endorphin (p < 0.001). The yellow obese phenotype was more sensitive than the black lean phenotype to the neurochemical effect of early postnatal MSG administration. Recent reports suggest the agouti locus protein is an antagonist of the receptor for another POMC peptide, melanocyte-stimulating hormone (MSH). Therefore, the balance of functional activity between various POMC peptides appears to be an important factor in the development of both acquired and genetic obesity.

Topics: Animals; Animals, Newborn; beta-Endorphin; Depression, Chemical; Dopamine; Drinking; Eating; Female; Hair Color; Hypothalamus; Mice; Mice, Inbred A; Mice, Inbred C3H; Mice, Inbred C57BL; Obesity; Organ Size; Phenotype; Pro-Opiomelanocortin; Rats; Sodium Glutamate; Weight Gain

This study was undertaken to investigate the effects of melanocortins and opioids on rat early postnatal body and organ growth. Among melanocortins tested desacetyl-alpha-melanocyte-stimulating hormone (alpha-MSH) at dosages of 0.3 and 3 micrograms/g/day was effective in stimulating neonatal growth with a weight gain of 7 and 5.6%, respectively, after 2 weeks of treatment. Likewise, a weight rise of 4.2 and 3% was obtained with 3 micrograms/g/day of both alpha-MSH and Nle4-D-Phe7 alpha-MSH. As far as opioids were concerned, while N-acetyl-beta-endorphin (beta-End) was ineffective, the activity of beta-End was dependent on dosage. Indeed, newborns treated with 0.03 microgram/g/day showed a slight, but significant, increase in weight, whereas a marked decrease in growth followed treatment with 0.3 and, mainly, 3 micrograms/g/day, with a final weight loss of 3.4 and 5.5%, respectively. All melanocortins exerted a positive action on muscular and brain trophism and, in addition, desacetyl-alpha-MSH also induced a rise of fat deposits. On the contrary, while the 0.03 microgram/g/day beta-End dose caused an increase in muscular and brain weight, the higher dosages of the opioid were detrimental, not only for muscle and brain, but also for both liver and spleen weight. A slight, although significant (P < 0.05), enhancement of serum dehydroepiandrosterone sulfate (DHEAS) level was found after the injection of 0.3 microgram/g desacetyl-alpha-MSH, whereas both the 0.3 and 3 micrograms/g doses of desacetyl-alpha-MSH and the 3 micrograms/g dose of alpha-MSH determined the rise of plasma androstenedione (P < 0.05). All tested melanocortins and opioids failed to modify the concentrations of corticosterone. Our results suggest that melanocortins and opioids can modulate early postnatal growth in rats either by direct or indirect mechanisms.

Topics: Adipose Tissue; alpha-MSH; Animals; beta-Endorphin; Body Weight; Brain; Dose-Response Relationship, Drug; Growth; Liver; Muscle, Skeletal; Organ Size; Rats; Spleen; Weight Gain; Weight Loss

The relationship between maternal plasma levels of beta-endorphin (beta-Ep) during labor and various obstetrical factors was investigated in 115 healthy pregnant women. beta-Ep was determined by radioimmunoassay using double-antibody RIA kit (INCSTAR Corporation, Stillwater, M'S.). The results were as follows: (1) The primiparous women showed a significant increase of maternal plasma levels of beta-Ep at delivery compared with the multiparous women. In addition, the group of women whose Bishop's score at the onset of labor was 5 points or less showed a significant increase of maternal plasma levels of beta-Ep at delivery compared with that in the group of women whose Bishop's score was 6 points or more. (2) The increase in maternal plasma levels of beta-Ep during the first and the second stage of labor was significantly higher in obese women (pre-pregnancy BMI > or = 24) than in normal weight women (pre-pregnancy BMI < 24). In normal weight women in pre-pregnancy, the group of women whose weight gain during pregnancy was 11kg or more showed a significantly higher increase of beta-Ep compared with that in the group of women whose weight gain was less than 11 kg. These results suggest that a stressful delivery caused a significant increase of maternal plasma levels of beta-Ep during labor. Moreover, obesity and marked weight gain during pregnancy caused a remarkable increase in beta-Ep probably due to latent dystocia.

Topics: beta-Endorphin; Female; Humans; Labor, Obstetric; Obesity; Parity; Pregnancy; Pregnancy Complications; Radioimmunoassay; Weight Gain

There is a considerable body of evidence to suggest that estrogen suppresses food intake and body weight gain by an action in the hypothalamus. However, the neurotransmitter/neuromodulator mediating the anorectic effects of estrogen are unknown. Neuropeptide-Y (NPY) is the most potent orexigenic signal known, and NPY-producing neurons in the hypothalamus concentrate 17 beta-estradiol (E2). In these studies we tested the hypothesis that estrogen-induced anorectic effects may be due to decreased NPY levels and release in hypothalamic sites previously implicated in the control of food intake. The results show that uninterrupted physiological levels of E2 in ovariectomized rats suppressed daily food intake and body weight gain. Evaluation of NPY concentrations in five hypothalamic sites showed that NPY levels were decreased selectively in the paraventricular nucleus (PVN) and neighboring perifornical nucleus of E2-treated rats. In contrast, concentrations of beta-endorphin, another less potent orexigenic peptide, were not changed by E2 in any hypothalamic site. In the next experiment, the effects of similar E2 treatment on NPY release in vitro from the PVN and ventromedial nucleus were studied in rats killed at the onset of the dark phase when food intake increases in conjunction with increased PVN NPY secretion. The results show that basal and KCl-induced NPY release were significantly decreased from the PVN of E2-treated compared to those in control rats. In contrast, both basal and KCl-induced NPY release from the ventromedial nucleus of E2-treated rats were similar to those in control rats. Collectively, these results show that estrogen suppresses NPY levels and release selectively from the PVN. As NPY levels and release in the PVN have been shown to be highly correlated with appetite status, and the PVN is one of the important sites of NPY action, these findings imply that the anorectic effects of estrogen may be mediated by decreased NPY release from the PVN NPY innervations.

Topics: Animals; Appetite Depressants; beta-Endorphin; Eating; Estradiol; Female; Hypothalamus; Neuropeptide Y; Paraventricular Hypothalamic Nucleus; Potassium Chloride; Rats; Weight Gain